4BBL1061 main exam practice paper

2022/3 Dr Greg Knock

This is the version with answers and explanations.

If you have not yet attempted the questions…

Look at the version without answers first.

If you have already looked at the version without answers and

had a go at answering them…

…and see how well you did.

The actual main exam will have 50 MCQs, (2 or 3 per lecture or practical).
This sample paper also has 50 MCQs.

For best results in the actual exam: STUDY THE LECTURES and
model answers for all practical and tutorial/PSW worksheets!
1. Which aspect of negative feedback control is most important in
maintaining a physiological variable within normal limits?
A. The response to a change reverses the change.
B. It has both sensors and effectors.
C. The response is always inhibitory.
D. The response to a change amplifies the change.
E. It can anticipate a change and respond before the change has
actually been sensed.

Answer = A (Lecture 2, homeostasis).

B. Not the best answer because this is also true for positive feedback.
C. No. The response can also be stimulatory, depending on whether the initial change was
an increase or a decrease in the variable being controlled.
D. No. This is positive feedback.
E. No. This is feed-forward.

2. Which component of all negative feedback loops carries information

from a sensor to the integrating centre?
A. A hormone.
B. The efferent pathway.
C. The afferent pathway.
D. The vagus nerve.
E. The effector.

Answer = C (L2, homeostasis). Simple fact.

A. Hormones do carry information but usually as part of a response (efferent pathway).
Also, not all negative feedback loops are hormonal.
B. No. This is the response pathway, from the integrating centre to the effector(s).
D. Not quite. The vagus nerve primarily carries efferent signals to effectors. Also, not ALL
negative feedback loops are neuronal.

C. No. The effector is what produces an effect (unsurprisingly 😊) in response to the

signal sent via the efferent pathway.
3. Which two features of muscle contraction are shared by skeletal,
cardiac, and smooth muscles?
A. An action potential propagating down the T tubular network to the
voltage sensor on the sarcoplasmic reticulum (SR) and Ca2+ release from
the SR.
B. An increase in intracellular Ca2+ concentration and hydrolysis of ATP.
C. Activation of myosin light-chain kinase by Ca2+/calmodulin and
hydrolysis of ATP.
D. Binding of Ca2+ to troponin C and movement of tropomyosin away
from the myosin binding site on actin.
E. An increase in intracellular Ca2+ concentration and phosphorylation
of troponin C.

Answer = B (Lecture 3, muscle cell function). Ca2+ is required to trigger contraction in

all muscle types and the force generated requires ATP.
A. This is only true for skeletal muscle. Cardiac muscle also has a T tubular network, but
no voltage sensor on the SR. Smooth muscle does not have a T tubular network or a voltage
sensor on the SR.
C. This is only true of smooth muscle. In skeletal and cardiac, Ca2+ binds to troponin C,
not calmodulin. Myosin light-chain kinase is only found in smooth muscle.
D. This is only true of skeletal and cardiac muscle. In smooth muscle, it is phosphorylation
of myosin-light chain by MLCK that triggers binding of myosin to actin.
E. All require an increase in Ca2+ but there is no troponin C in smooth muscle.

4. Which feature of excitation-contraction coupling in most types of

vascular smooth muscle is NOT shared by cardiac muscle?
A. Time-independent ion channels.
B. Voltage-dependent ion channels.
C. Actin-myosin cross-bridge cycling.
D. Hydrolysis of ATP.
E. Ca2+ influx.
Answer = A (L3, muscle cell function). Most types of vascular smooth muscle need to
maintain various degrees of contractile tone for very long periods of time. Thus, they
require sustained increases in intracellular Ca2+. The main source of this Ca2+ is via voltage-
gated ion channels. These channels need to remain open, so are time independent (they
are not inactivated by prolonged depolarisation as in neurons and cardiac muscle).
B, C, D and E are all true statements of features shared by vascular smooth muscle and
cardiac muscle.

5. Accumulation of thick sticky mucus in airways, intestines and

pancreatic duct is caused by:
A. Proliferation of epithelial cells due to adherens junction dysfunction.
B. Mutation of epithelial CFTR channel preventing secretion of water
into the tubular lumen.
C. Proliferation of goblet cells.
D. Paralysis of cilia by cigarette smoke.
E. Mutation of epithelial CFTR channel preventing absorption of water
from the tubular lumen.

Answer = B (Lecture 4, epithelial cell function). Thick sticky mucus accumulation is

characteristic of cystic fibrosis which is caused by a loss-of-function mutation in the cystic
fibrosis transmembrane regulator on epithelial cells lining the lumen of intestines, airways
and secretory ducts.
A. No. This occurs in some cancers but is not associated with thick sticky mucus.
C. No. This occurs in airways of sufferers of asthma and there is excess mucus produced
but it is otherwise normal.
D. No. Smoking paralyses cilia in airways, causing mucus to accumulate, but not in
intestines and pancreatic duct.
E. No. The mutation prevents water being secreted into the lumen of the tube, not
absorption from the lumen of the tube.
6. In which two tissues might you find ciliated epithelium?
A. Alveoli and fallopian tube.
B. Upper airways and ileum.
C. Upper airways and renal proximal tubule.
D. Upper airways and fallopian tube.
E. Fallopian tube and renal proximal tubule.

Answer = D (L4: epithelial function). Upper airways and fallopian tubes are ciliated. Cilia
are there to sweep the contents of the tube along the tube. In upper airways: up to the
back of the throat. In fallopian tube: to the uterus.
A. Smaller bronchioles and alveoli are not ciliated. Instead, they have macrophages to
remove foreign particles.
B. Ileum and other parts of the digestive tract have microvilli to maximise surface area
for absorption. They do not need cilia. Movement is by peristalsis.
C. The renal PCT has microvilli to maximise surface area for reabsorption. They do not
need cilia. Movement is by filtration pressure.
E. No. Not renal PCT, As in C.

7. In the cardiac cycle, what happens next after the aortic valve closes?
A. The mitral valve closes.
B. Filling.
C. Isovolumetric contraction.
D. Isovolumetric relaxation.
E. Ejection.

Answer = D (L5 cardiac cycle). The aortic valve closes after blood has been ejected into
the aorta (through the aortic valve). The muscle needs to relax before the next filling can
occur.
A. No. The mitral valve is already closed at this point.
B. No. The muscle needs to relax before the next cycle of filling can occur.
C. No. This occurred before the aortic valve opened.
E. No. Eject had occurred just before the aortic valve closed.
8. When the heart contracts, what can be measured to calculate stroke
work (energy expenditure of the contracting muscle)?
A. Aortic pressure.
B. The change in pressure during isovolumetric contraction.
C. The difference between end-systolic and end-diastolic volume.
D. The change in pressure during isovolumetric relaxation.
E. The area of the pressure-volume loop.

Answer = E (Lecture 5, cardiac cycle). The pressure volume loop is a plot of changes in
ventricular pressure (vertical axis) against changes in ventricular volume (horizontal axis).
The bigger the area of the loop, the harder the heart is working.
A. No. Aortic pressure will increase with increased work, but pressure is not the sole
determinant.
B. No. but this is one of the components of the pressure volume loop.
C. No, but this is one of the components of the pressure volume loop (stroke volume).
D. No, but this is one of the components of the pressure volume loop.

9. Which vessels carry non-filtered plasma away from the site of renal
filtration?
A. Afferent arterioles.
B. Proximal convoluted tubules.
C. Glomerular capillaries.
D. Efferent arterioles.
E. Peritubular capillaries.

Answer = D (Lecture 6, kidney function). The site of filtration is of course the

glomerulus. The efferent arteriole carries blood (containing unfiltered plasma) AWAY from
the glomerulus.
A. No. This carries blood INTO the glomerulus for filtration.
B. No. This is the first main segment of the nephron. Filtrate flows into it from the
Bowman’s capsule that surrounds the glomerulus.
C. No. This is the site of filtration.
E. No. These are the site of exchange of secreted and/or reabsorbed substances to/from
the various parts of nephron.

10. Reabsorption of glucose in the nephron requires the active transport

of Na+ by which transporter?
A. Apical Na+/K+ ATPase.
B. Apical SGLT (Na+/glucose co-transporter).
C. Basolateral GLUT.
D. Basolateral SGLT (Na+/glucose co-transporter).
E. Basolateral Na+/K+ ATPase.

Answer = E (Lecture 6, kidney function). The pumping of Na+ out of the cell into the
interstitium sets up a Na+ gradient within the cell which facilitates the absorption of
glucose from filtrate into the cell. See tutorial 1.
A. No. This is not expressed on the apical surface. If it was, it would oppose the absorption
of Na+ and nutrients.
B. This is the transporter that brings glucose into the cell from the filtrate, but it uses
facilitated diffusion, not active transport.
C. This is the transporter that carries glucose from the cell into the interstitium, but it
uses facilitated diffusion, not active transport.
D. No, for reasons stated above. Also wrong because SLGLT is only expressed on the apical
surface (not the basolateral surface).

11. Which two haemodynamic factors, if increased, would both contribute

to an increase in stroke volume?
A. Blood volume and venous capacitance.
B. venous capacitance and heart rate.
C. Venous capacitance and ventricular contractility.
D. Blood volume and ventricular contractility.
E. Central venous pressure and muscle blood flow.
Answer = D (Lecture 7, control of cardiac output). There are three main contributing
factors to an increased stroke volume: increased blood volume, increased central venous
pressure (and therefore increased venous return) and increased cardiac contractility.
A. Blood volume yes, but an increased venous capacitance would decrease central venous
pressure, thus reducing venous return.
B. Not venous capacitance, as explained above. Heart rate is the other contributor to
cardiac output and does not contribute directly to stroke volume.
C. Ventricular contractility yes, but not venous capacitance, as explained above.
E. Central venous pressure yes, but an increased muscle blood flow is one possible
consequence of increased stroke volume, not a cause of it.

12. What is sensed by the kidney to result in the secretion of less

aldosterone by the adrenal cortex?
A. Decreased glomerular filtration rate.
B. Increased mean arterial blood pressure.
C. Increased glomerular filtration rate.
D. Increased plasma osmolality.
E. Decreased blood volume.

Answer = C (Lecture 7, control of blood pressure). The renin angiotensin aldosterone

system is involved in the long-term regulation of MAP through control of blood volume.
Aldosterone promotes an increase in blood volume by stimulating the reabsorption of more
Na+ (and therefore more water) in the kidney. For there to be less aldosterone being
secreted, there must have been an increase in blood volume above the normal level. The
kidney sensed changes in blood volume indirectly through changes in glomerular filtration
rate (GFR). If volume had increased, then GFR would have increased too.
A. No. A decreased GFR would result in more aldosterone being secreted.
B. Not quite. An increased MAP would be associated with an increased GFR, but the kidney
does not directly sense MAP. It senses changes in MAP indirectly via GFR.
D. No. Aldosterone has nothing to do with osmolality control. ADH is the main hormone
involved in control of osmolality (also acting on the kidney).
E. No. A decreased blood volume (via decreased MAP and decreased GFR) would result in
more aldosterone being secreted, not less.
13. What would you expect cerebral arterioles do in response to
haemorrhage and why?
A. Dilate, to maintain blood flow to the brain despite a fall in MAP.
B. Constrict to maintain blood flow to the brain despite a fall in MAP.
C. Dilate, to maintain blood flow to the brain despite an increase in
MAP.
D. Constrict, to maintain blood flow to the brain despite an increase in
MAP.
E. Nothing because haemorrhage will not influence brain blood flow.

Answer = A (Lecture 8, control of blood flow). The brain can regulate its own blood flow.
It needs to do so to prevent brain damage. During haemorrhage, blood volume falls,
therefore venous return, stroke volume, cardiac output, and MAP fall. To compensate for
the drop in cerebral perfusion pressure and maintain cerebral blood flow, cerebral
arterioles dilate.
B. No. Constriction would further reduce brain blood flow. This would happen in response
to an increase in CO and MAP, not a decrease.
C. Dilate yes, but haemorrhage does not increase MAP. It decreases it.
D. No. Constriction will compensate for an increase MAP, but haemorrhage decreases MAP,
as explained above.
E. No. Haemorrhage does influence brain blood flow, as explained above.

14. If cardiac output doubled and total peripheral resistance decreased by

50%, what would happen to total lung blood flow?
A. It would double.
B. It would not change.
C. It would increase by 50%.
D. It would decrease by 50%.
E. It would increase four-fold.

Answer = A (Lecture 8, control of blood flow). The ONLY determinant of total lung blood
flow is cardiac output. Cardiac output (CO) is the total blood flow out of BOTH ventricles
(LV for the systemic circulation and RV for the pulmonary circulation). Therefore, if CO
doubles, lung blood flow doubles. Total peripheral resistance is the sum of all resistances
in the systemic circulation. It is independent of CO. It influences MAP (total pressure in
the systemic circulation) but has no influence over lung blood flow or pulmonary artery
pressure.
B. No. If CO changes, lung blood flow MUST change in the same direction and by the same
amount.
C. No. For same reason as given above.
D. No. For same reason as given above.
E. No. For same reason as given above.

15. During moderate exercise, cardiac output is doubled, but mean

arterial blood pressure only increases by a few mm Hg. Why is this?
A. There is only a small increase in total peripheral resistance through
vasoconstriction.
B. There is also a big drop in total peripheral resistance through
vasoconstriction in muscle and skin.
C. There is also a big drop in total peripheral resistance through
vasodilation in muscle and skin.
D. Mean arterial pressure is independent of cardiac output.
E. There is only a small decrease in total peripheral resistance through
vasodilation.

Answer = C (L9, introduction to practicals, practical 1). MAP = CO x TPR. This means
that an increase in either CO or TPR, or both, will increase MAP. However, if CO is increased
but there is a compensatory decrease in TPR, MAP will not change or only change slightly.
During moderate exercise, the big increase in CO is compensated for by a not quite so big
drop in TPR, so MAP only increases slightly. The drop in TPR is caused by vasodilation in
muscle (to increase muscle blood flow) and skin (to prevent overheating).
A. No. Vasoconstriction would raise TPR, but TPR does not increase during exercise. It
decreases, as explained above.
B. No. There is a big drop in TPR, but it is caused by vasodilation in muscle and skin, not
vasoconstriction.
D. No. MAP is dependent on both CO and TPR: MAP = CO x TPR.
E. No. Vasodilation does lower TPR, but it is not a small drop. It is a big drop, as explained
above.
16. From the electrocardiogram above, calculate average heart rate in
beats per minute (bpm).
A. 60 bpm.
B. 77 bpm.
C. 47 bpm.
D. 66 bpm.
E. 86 bpm.
Answer = B (L9, practical 1). Heart rate in beats per minute is calculated from the ECG
using the formula: HR = 60/R-R interval (in sec). The ‘R’ wave is the tallest and most
short-lived component of the ECG. The R-R interval is the time between adjacent R waves.
There are five R waves visible, but only four complete R-R intervals. The average duration
of those four intervals is 0.783 sec. 60/0.783 = 76.6 (rounded to 77 bpm).
17. If diastolic blood pressure is 87 mmHg and systolic blood pressure is
136 mmHg, what is mean arterial blood pressure?
A. 111.5 mmHg.
B. 103.3 mmHg.
C. 74.3 mmHg.
D. 161.3 mmHg.
E. 49 mmHg.

Answer = B (L9, practical 1). MAP is calculated from DBP and SBP using the formula: MAP
= DBP + (SBP-DBP)/3.

18.When the diaphragm contracts, what happens to intrapleural pressure

and then to alveolar pressure?
A. Neither change at all.
B. Intrapleural pressure increases and alveolar pressure decreases.
C. They both decrease.
D. They both increase.
E. Intrapleural pressure decreases and alveolar pressure increases.

Answer = C (L10, lung function). The diaphragm contracts when we are breathing in. It
increases the volume of the chest cavity. This causes a pressure drop first in the
intrapleural space and then inside the alveoli. It is the pressure drop in the alveoli that
allows air to flow into the lungs.
A. No. If neither changed there would not be any airflow.
B. No. If one increases the other will increase.
D. No. This occurs during expiration when the diaphragm relaxes.
E. No. If one decreases the other will decrease.
19. Why does lack of surfactant make it more difficult to breath normally?
A. Without surfactant, larger alveoli are more likely to collapse, so
more effort is required to expand the lungs.
B. Without surfactant, airways are more likely to actively constrict, so
airflow is obstructed.
C. Without surfactant, alveolar surface tension is reduced, so more
effort is required to expand the lungs.
D. Without surfactant, smaller alveoli are more likely to collapse, so
more effort is required to expand the lungs.
E. Lack of surfactant makes the lungs dry out.

Answer = D. (L10, lung compliance). The amount of effort required to expand the lungs
is inversely proportional to lung compliance. The more compliant lung tissue is, the more
easily it can be expanded. Surfactant increases compliance by reducing alveolar surface
tension and prevent smaller alveoli from collapsing. Thus, in the absence of surfactant,
smaller alveoli will collapse and much more effort is required to expand the lungs
(compliance is reduced) – it is more difficult to breath normally.
A. No. It is smaller alveoli that will collapse, not larger alveoli. The rest is correct.
B. No. Surfactant does not influence active constriction/relaxation of airways. It
influences compliance, not resistance to airflow.
C. No. Lack of surfactant would increase surface tension, not decrease it.
E. No. There is still fluid lining the alveoli. Surfactant is just one component of it.

20. If a subject had 50% of the normal haemoglobin content in their blood,
what would you expect their resting arterial PO2 to be?
A. It should be normal at 13.3 kPa.
B. It should be approximately halved at 6 kPa.
C. It should be approximately halved at 7 kPa.
D. It should be reduced by about 1.7 kPa below the normal resting level.
E. It should be normal at 12.5 kPa.

Answer = E (L11, O2 transport). Normal arterial PO2 at rest is 12.5 kPa on average.
Reduced Hb content occurs in anaemia. This reduces the O2 carrying capacity of blood.
Thus, for a given PO2, O2 content is halved. However, in anaemia, lung function is normal,
diffusion of gases in the lungs is normal, so PO2 of blood flowing through the lungs
equilibrates with alveolar air as normal. It is not influenced by Hb content.
A. No. 13.3 kPa is the value at which PO2 first equilibrates in the lungs. It drops to 12.5
kPa as it flows back to the heart due to the addition of some deoxygenated blood from
respiring airways.
B. No. It is O2 content that is halved, not PO2.
C. No. It is O2 content that is halved, not PO2.
D. No. This is what might be expected to occur in mixed venous blood, not arterial.

21. How does deoxygenation of blood increase the rate at which CO2 is
converted to bicarbonate in blood?
A. Reduced O2 content means there is space for more CO2 in blood, so
more CO2 can be absorbed into blood and converted to bicarbonate.
B. Deoxygenation increases the H+ buffering capacity of haemoglobin.
C. Deoxygenation reduces the H+ buffering capacity of haemoglobin.
D. Deoxygenation increases the rate at which CO2 can chemically react
with haemoglobin.
E. Reduced PO2 directly increases the activity of carbonic anhydrase in
erythrocytes.

Answer = B (L11, CO2 transport). This is part of the Haldane effect that describes how
deoxygenation of blood increases the uptake of CO 2 by blood in respiring tissues.
Bicarbonate = HCO3-. It is in equilibrium with CO2 in solution. Removal of more H+ from
solution by Hb shifts the equilibrium CO2 + H2O → HCO3- + H+ to the right, favouring the
production of more bicarbonate and H+ from CO2 and H2O.
A. No. The term ‘gaseous exchange’ is misleading. We don’t literally have ‘exchange’ of
O2 for CO2. O2 and CO2 diffuse down their own partial pressure gradients independently of
each other.
C. No. It is the other way around as explained above.
D. A true statement, but this does not increase the rate of bicarbonate formation. It
increases the rate of carbamino formation. This is the other component of the Haldane
effect.
E. No. Carbonic anhydrase is the enzyme that facilitates the interconversion of CO 2 and
bicarbonate, but its activity is not directly influenced by PO2.
22. Under what conditions would we expect expiratory neurons to be
active?
A. Any situation where ventilation needs to be increased above the
normal resting level.
B. During every breath out.
C. Only when the subject is at rest.
D. Only at high altitude.
E. Only during exercise.

Answer = A. (L12, control of breathing). Expiratory neurons are responsible for

stimulating expiratory muscles. At rest, only inspiratory neurons are active because during
normal expiration elastic recoil of the lungs is enough to force air out – no contraction of
expiratory muscles is required. When ventilation needs to be increased (for whatever
reason) we then have alternative stimulation of inspiratory and expiratory muscle through
alternative firing of inspiratory and expiratory neurons.
B. No. not at rest – only when ventilation needs to be increased.
C. No. not at rest – only when ventilation needs to be increased.
D. It will be required at high altitude, but not ONLY at high altitude.
E. It will be required during exercise, but not ONLY during exercise.

23. At high altitude, what is the main resting determinant of ventilation

rate?
A. Arterial PCO2.
B. Arterial PO2.
C. Arterial PO2 and arterial PCO2 in equal measure.
D. Mixed venous PCO2.
E. Mixed venous PO2.

Answer = B. (L12, control of breathing). At sea level the most important determinant of
ventilation rate is arterial PCO2. However, at high altitude, the air is thinner, so PO2 of
inspired air is greatly reduced. This results in greatly reduced arterial PO2. When arterial
PO2 falls below around 8 kPa, it becomes the most important stimulus for ventilation.
A. No. At high altitude, resting metabolic demand remains normal, so resting CO 2
production is normal and resting PCO2 remains normal.
C. No, not at rest. A simultaneous increase in PCO2 would only occur if metabolic demand
was also increased, such as through exercise. Then a drop in PO2 and an increase in PCO2
would act synergistically to stimulate ventilation.
D. No. PCO2 is only measured in arterial blood by the central and peripheral
chemoreceptors.
E. No. PO2 is only measured in arterial blood by the peripheral chemoreceptors.

24. From the spirometer trace above, determine vital capacity.

A. 2.7 L
B. 1.2 L
C. 3.4 L
D. 4.6 L
E. 5.0 L
Answer = D (L9, introduction to practicals, practical 2). Vital capacity is the volume you
can breathe in from maximum breath out up to maximum breath in. On the trace, it is the
difference between the highest point and the lowest point.
A. No. This is inspiratory reserve volume (from top of a normal breath in up to maximum
breath in).
B. No. This is expiratory reserve volume (from bottom of normal breath out to bottom of
maximum breath out).
C. No. This is inspiratory capacity (Sum of tidal volume and inspiratory reserve volume).
E. No. This is VC multiplied by 1.09. You only need to multiply by 1.09 to convert from
ATPS (atmospheric temperature) to BTPS (body temperature). This trace already shows
the volume at BTPS.

25. Using the same spirometer trace as for Q24, calculate minute
ventilation from the first five breaths on the trace.
A. 0.7 L.
B. 3.5 L/min.
C. 15 breaths per minute.
D. 10.5 L.
E. 10.5 L/min.

Answer = E (L9, practical 2). Ventilation is flow of air in and out of the lungs. Flow is
measured in litres per minute. Ventilation is calculated by multiplying tidal volume (in L)
by breathing rate (in breaths per minute). The volume of each of the first five breaths is
0.7 L. This is tidal volume. The five breaths occur over 20 seconds, so breathing rate = 5
x 3 = 15 breaths per minute (i.e., in 60 seconds). Therefore, minute ventilation = 0.7 x 15
= 10.5 L/min.
A. No. This is tidal volume.
B. No. This is volume in 20 seconds. Minute ventilation is volume in 60 seconds.
C. No. This is breathing rate.
D. No. The units are wrong. L is simply a volume. Flow is measured in L/min.
26. The vitalograph trace above was produced when a subject took a
maximum breath in and blew into the device as hard and fast as they could
for 6 seconds. What can you say about the health of the subject who
recorded this vitalograph?
A. They appear to have an obstructive lung disease.
B. They appear to have a restrictive lung disease.
C. They appear to have healthy lungs.
D. They probably have asthma.
E. They probably have chronic obstructive lung disease.

Answer = A (L9, introduction to practicals, practical 2). Obstructive lung disease is

indicated by a low (<50%) forced expiratory ratio (FER). FER is calculated by dividing
forced expiratory volume in 1 second (FEV1) by forced vital capacity (FVC, the maximum
volume on the trace). From this trace, FEV1 = 2L and FVC = 4.4L, thus FER = 2/4.4 = 0.45
(45%).
B. No. This would be suggested by a high (>70%) FER, but even then, it would not
necessarily be a positive diagnosis. Further tests would be required.
C. No. Healthy FER is typically around 75%.
D. No. Asthma is a type of obstructive lung disease, but we cannot say which type it is
from the trace alone. Further tests would be required.
E. No. COPD is a type of obstructive lung disease, but we cannot say which type it is from
the trace alone. Further tests would be required.

27. What is the main source of ATP during middle distance running?
A. Oxidative phosphorylation of stored fat only.
B. Glycolysis from glycogen stores only.
C. Mainly glycolysis but supplemented with oxidative phosphorylation
of acetyl-CoA derived from glycogen and fat.
D. ATP and phosphocreatine stored in muscle.
E. ATP isn’t required for middle distance running.

Answer = C (L13, exercise physiology). During middle distance running, glycogen is the
primary source of fuel because it is not likely to be depleted during the run and can be
rapidly metabolised through glycolysis to make ATP. Nevertheless, while fat metabolism
alone is too slow to keep up with metabolic demand, some fat is utilised. In addition to
glycolysis, both fuels are more slowly but fully metabolised through oxidative
phosphorylation to make more ATP.
A. No. This is only sustainable during low intensity exercise for very long periods. Long-
distance running utilises both glycogen and stored fat for oxidative phosphorylation.
B. No. During running, there is always glycolysis and oxidative phosphorylation. It is the
relative reliance on one or the other that varies depending on the required level of
exercise intensity and duration.
D. No. Stored ATP and phosphocreatine are depleted with ~10 seconds, so only good for
short sprints or weightlifting. Beyond that short time, new ATP must be made from stored
fuels.
E. No. There is an absolute requirement for ATP in all types of muscle contraction during
all types of exercise.
28. During constant load exercise, which parameter reaches a steady state
first?
A. Cardiac output.
B. Heart rate.
C. Work rate.
D. Ventilation.
E. Oxygen delivery (VO2).

Answer = C (L13, exercise physiology). When undergoing constant load exercise 9such
as on a treadmill set at a fixed speed). Work rate reaches a steady state within seconds.
It will take all other parameters several minutes to ‘catch up’.
A, B, D, E. All of these will reach a steady state but only after a lag period. This delay is
the cause of the O2 deficit that must then be repaid when exercise stops.

29. From where is CRH produced and what does it act on?
A. The adrenal cortex and various tissues of the body.
B. The posterior pituitary and the adrenal cortex.
C. The anterior pituitary and the adrenal cortex.
D. The hypothalamus and cortisol secreting cells of the anterior
pituitary.
E. The hypothalamus and ACTH secreting cells of the anterior pituitary.

Answer = E. (L15 hypothalamus and pituitary). CRH = corticotrophin releasing hormone.

All releasing hormones are produced in the hypothalamus. They are secreted into the
portal system where blood carries them down the pituitary stalk to the anterior pituitary
gland. CRH stimulates the secretion into the blood of ACTH (adrenocorticotropic hormone)
from the pituitary.
A. No. cortisol is secreted from the adrenal cortex and acts on various tissues of the body.
B. No. Only ADH and oxytocin are secreted from the posterior pituitary. Releasing
hormones don’t act on the posterior pituitary.
C. No. ACTH is secreted from the anterior pituitary and acts on the adrenal cortex to
stimulate cortisol secretion.
D. Only partly correct. CRH is secreted by the hypothalamus but there are no cortisol
secreting cells in the pituitary.
30. What is oxytocin?
A. A steroid hormone synthesised in the adrenal cortex and acting on
the uterus.
B. A peptide hormone synthesised in the posterior pituitary and acting
on the uterus.
C. A peptide hormone synthesised in hypothalamic neurones and
secreted from the anterior pituitary.
D. A peptide hormone synthesised in hypothalamic neurons and
secreted from the posterior pituitary.
E. A steroid hormone synthesised in hypothalamic neurones and
secreted from the posterior pituitary.

Answer = D (L15, hypothalamus and pituitary). Oxytocin and ADH are both peptide
hormones made in the hypothalamus. They are packaged in vesicles that are transported
down nerve fibers to the posterior pituitary gland from where they are secreted into the
blood.
A. No. Oxytocin does act on the uterus, but it is not a steroid and not made in the adrenal
gland.
B. No. It is released from the posterior pituitary but is made in the hypothalamus.
C. No. It is secreted from the posterior pituitary, not the anterior pituitary.
E. No. It is not a steroid hormone.

31. What is pituitary dwarfism?

A. Subjects of short stature in adulthood caused by a lack of growth
hormone.
B. A small pituitary gland caused by a lack of growth hormone.
C. Subjects of short stature in adulthood caused by a lack of
somatostatin.
D. Subjects of short stature in adulthood caused by too much GHRH.
E. Subjects of short stature caused by a mutation in the fibroblast
growth-factor receptor (FGFR).

Answer = A (L15, hypothalamus and pituitary). Normal stature in adulthood requires

continuous secretion of the correct levels of growth hormone from the pituitary gland in
response to GHRH from the hypothalamus. This is especially important during puberty.
Without growth hormone, subjects remain of prepubescent stature well into adulthood.
B. No. GH does not influence the size of the pituitary gland.
C. No. somatostatin inhibits GH secretion from the pituitary, so a lack of SS would
stimulate the secretion of too much GH – potentially causing giantism.
D. No. GHRH (growth hormone releasing hormone) from the hypothalamus stimulates GH
secretion from the pituitary, so too much GHRH would result in too much GH.
E. No. FGFR mutation causes the other more common type of dwarfism, achondroplasia.
It is not associated with abnormal GH secretion.

32. When and how is gluconeogenesis most likely to occur?

A. In the absorptive state, in response to an increased secretion of
glucagon.
B. In the post-absorptive state, in response to an increased secretion
of glucagon.
C. In the post-absorptive state, in response to an increased secretion
of insulin.
D. In the absorptive state, in response to an increased secretion of
insulin.
E. In the post-absorptive state, in response to a decreased secretion of
adrenaline.

Answer = B (L16, fuel homeostasis). Gluconeogenesis is the conversion of amino acids

and glycerol into glucose in the liver. This is stimulated by glucagon and occurs in the post-
absorptive (fasting) state to help maintain plasma glucose concentration despite the
absence of dietary glucose.
A. No. In the absorptive state gluconeogenesis is not needed. There is an excess of glucose
being absorbed from the GI tract and glucagon secretion is at its lowest level.
C. No. Gluconeogenesis is not stimulated by insulin and insulin secretion is at its lowest
during the post-absorptive state.
D. No. In the absorptive state gluconeogenesis is not needed. There is an excess of glucose
being absorbed from the GI tract.
E. No. Adrenaline secretion increases in response to decreased plasma glucose, so it can
then stimulate gluconeogenesis.
33. What three key actions of insulin help prevent plasma glucose
concentration from going too high?
A. Stimulation of gluconeogenesis in liver and stimulation of uptake of
glucose by adipose and muscle.
B. Stimulation of uptake of glucose by liver, adipose and muscle.
C. Stimulation of glycogenolysis in liver and stimulation of uptake of
glucose by adipose and muscle.
D. Stimulation of lipolysis in adipose, stimulation of proteolysis in
muscle and stimulation of glycogenolysis in liver.
E. Stimulation of glycogenesis in liver and uptake of glucose by adipose
and muscle.

Answer = E (L16, tutorial 4, fuel homeostasis). Insulin is an anabolic hormone. It

promotes storage of fuel during the absorptive state. Glycogenesis is the formation of
glycogen from glucose taken up from the plasma. Glucose transport in adipose and muscle
requires insulin.
A. No. Insulin does stimulate glucose uptake in adipose and muscle, but it does not
stimulate gluconeogenesis.
B. No. Glucose uptake in liver occurs constitutively. It does not require insulin to activate
the transporter.
C. No. Insulin does not stimulate glycogenolysis. It does the opposite (glycogenesis).
D. No. Lipolysis, proteolysis and glycogenolysis are all catabolic processes and all occur in
the post-absorptive state. They are not stimulated by insulin.

34. Assuming a renal transfer maximum Tm for glucose of 10 mM, after a

bolus of glucose was given to a diabetic subject, plasma glucose
concentration peaked at 16 mM. At what concentration would urinary
glucose concentration reach its peak?
A. Zero.
B. 10 mM.
C. 16 mM.
D. 13 mM.
E. 6 mM.
Answer = E (L17, tutorial 4, diabetes). The transfer maximum is the maximum
concentration of plasma glucose that can be filtered and still all be reabsorbed in the
proximal convoluted tubule. If plasma glucose peaks at 16 mM and the transfer maximum
is 10 mM, then any excess glucose over 10 mM cannot be reabsorbed and ends up in the
urine. 16 – 10 = 6 mM.

35. Why does type 1 diabetes cause weight loss?

A. Without insulin, catabolism in adipose and muscle are both greatly
increased.
B. Diabetics suffer from loss of appetite, so food intake is greatly
reduced.
C. Without insulin, renal function is greatly impaired, so much less
glucose is reabsorbed in the proximal convoluted tubule.
D. Lack of insulin causes chronic vomiting and diarrhoea.
E. Without insulin, anabolism in adipose and muscle are both greatly
increased.

Answer = A (L17, diabetes). Insulin is an anabolic hormone. It promotes the storage of

glucose as fat in adipose and as glycogen in liver and muscle. It also promotes tissue
growth. Without insulin, glucose cannot be utilised by tissues and catabolism dominates
(lipolysis, proteolysis, glycogenolysis).
B. No. Appetite, if anything, will be increased but with little effect.
C. No. General renal dysfunction is a long-term complication of diabetes, but renal Tmax
for glucose is normal (see Q25).
D. No. GI tract function is normal.
E. No. Catabolism is increased. Anabolism is decreased.
36. Why are type 2 diabetics more likely to be obese than non-diabetics?
A. Type two diabetics have an underactive thyroid gland.
B. Obesity is the main cause of insulin resistance in type 2 diabetes.
C. Insulin resistance increases the ability of adipose to store fat.
D. Insulin resistance increases appetite.
E. Lack of insulin increases the ability of adipose to store fat.

Answer = B (L17, diabetes). Type 2 diabetes is characterised by insulin resistance and

obesity causes insulin resistance. Obesity is not caused by diabetes (of either type).
A. Not really. Low metabolic rate could be a cause of the obesity, but the cause of the
obesity is irrelevant to the onset of type 2 diabetes. Many type 2 diabetics will have normal
thyroid function.
C. No. Obesity causes insulin resistance, not the other way around.
D. No. Increased appetite is one possible cause of obesity which can then lead to type 2
diabetes.
E. No. Lack of insulin occurs in type 1 diabetes. Without insulin adipose cannot take up
glucose, therefore adipose cannot make and deposit fat.

37. If a subject has a blood glucose concentration below the normal range
and blood ketone levels around 20 times the normal range, what is the
likeliest explanation?
A. The subject had just eaten a meal high in protein but very low in
carbohydrate.
B. The subject was suffering from type 1 diabetes.
C. The subject was suffering from type 2 diabetes.
D. The subject had undergone a long period of sustained fasting.
E. The subject had been hyperventilating.

Answer = D (practical 3). During prolonged fasting, no carbohydrate is being absorbed

from the GI tract and glycogen stores are being depleted, so blood glucose falls. Lipolysis
and muscle breakdown are stimulated. Fatty acids are used to make ketones, an
alternative energy source to glucose. Blood ketone levels increase several-fold.
A. No. Such a diet is unlikely to lower blood glucose unless every meal is of that sort. High
dietary protein has no influence over ketone production.
B. No. Diabetes is clearly indicated by a sustained higher than normal blood glucose level.
C. No. Diabetes is clearly indicated by a sustained higher than normal blood glucose level.
E. No. Hyperventilation is an effect of ketoacidosis, not a cause of it.

38. What do thyroid hormones and catecholamines have in common?

A. They are all derived from the amino acid tyrosine.
B. They are all derived from the amino acid threonine.
C. They are all steroid hormones.
D. They are all peptide hormones.
E. They all lower blood pressure.

Answer = A (L18, thyroid function). T3 and T4 are derived from tyrosine. So are the
catecholamines adrenaline and noradrenaline.
B. No. Tyrosine.
C. No. Tyrosine derivatives.
D. No. Tyrosine derivatives.
E. No. Through different mechanisms they all may increase blood pressure if produced in
excess over long periods of time.

39. What is a major consequence of iodine deficiency?

A. TSH deficiency.
B. Tachycardia.
C. Increased metabolic rate.
D. Grave’s disease.
E. Hypothyroidism.

Answer = E (L18, Thyroid function). Iodine is required for the synthesis of thyroid
hormones (T4/T3). Thus, iodine deficiency results in lack of thyroid hormone =
hypothyroidism.
A. No. TSH is thyroid stimulating hormone, secreted by the pituitary gland. It does not
require iodine for its synthesis. In fact, there will be more TSH than normal due to the
lack of negative feedback by T3/T4.
B. No. Tachycardia is a consequence of hyperthyroidism because T3/T4 increase sensitivity
of the SA node to catecholamines, increasing heart rate above normal.
C. No. increased metabolic rate is a consequence of hyperthyroidism because T3/T4
increase catabolic processes such as glycogenolysis.
D. No. Grave’s disease is a type of hyperthyroidism caused by over-activation of the TSH
receptor by an auto-antibody, resulting in too much T3/T4 being made.

40. How does thyroid hormone influence gene expression?

A. By binding to a membrane bound G-protein coupled receptor and
activating adenylate cyclase.
B. By binding to a nuclear receptor which then binds to the hormone
response elements on the gene.
C. By binding to a membrane bound G-protein coupled receptor and
activating phospholipase C.
D. By binding to a cytosolic receptor and then translocating to the
nucleus.
E. By binding to a cytosolic receptor which then binds to the hormone
response element on the gene.

Answer = B (L18, thyroid function). Thyroid hormone diffuses across the plasma
membrane into the nucleus where it binds to its receptor. The receptor then complexes
with the RXR receptor to activate the hormone response element on the gene.
A. No. Thyroid hormones do not bind to cell surface receptors.
C. No. Thyroid hormones do not bind to cell surface receptors.
D. No. This is how steroid hormones influence gene expression.
E. No. Both thyroid hormone receptors and hormone response elements are in the nucleus.
41. What would be the effect of increased secretion of anti-diuretic
hormone from the pituitary gland?
A. More water would be reabsorbed in the kidney resulting in an
increased plasma osmolality.
B. More water would be reabsorbed in the kidney resulting in a
decreased plasma osmolality.
C. More salt would be reabsorbed in the kidney resulting in an increased
plasma volume.
D. Less water would be reabsorbed in the kidney resulting in a
decreased plasma osmolality.
E. Less water would be reabsorbed in the kidney resulting in an
increased plasma osmolality.

Answer = B (L19 and tutorial 4, ADH and the control of osmolality). Osmolality is a
measure of the relative solute concentration in fluids such as plasma and renal filtrate.
Osmolality is regulated by ADH. ADH promotes the reabsorption of water back into the
blood from the renal collecting duct. If plasma osmolality fell, less ADH would be secreted
and less water would be reabsorbed, bringing plasma osmolality back up. If plasma
osmolality rose, the reverse would occur to bring plasma osmolality back down.
A. No. ADH promotes water reabsorption, but if more water was reabsorbed, osmolality
would fall because water dilutes the solutes.
C. No. More salt being reabsorbed would result in an increased plasma volume, but salt
reabsorption in the kidney is controlled by aldosterone not ADH.
D. No. Only a decreased secretion of ADH would result in less water being reabsorbed and
less water being reabsorbed would increase plasma osmolality, not decrease it.
E. No. Only a decreased secretion of ADH would result in less water being reabsorbed.

42. What would be an effect of inhibiting the active transport of Na+ out
of the thick ascending loop of Henle?
A. Failure of the separation of water and salt reabsorption.
B. More water can be reabsorbed from the collecting duct.
C. Impaired reabsorption of nutrients in the kidney.
D. Nothing. There is no active transport of Na+ in that part of the loop.
E. Interstitial fluid would become more concentrated the deeper into
the medulla the loop descended.
Answer = A ((L19 and tutorial 4, ADH and the control of osmolality). The thick ascending
loop is impermeable to water, so when Na+ is pumped out of the filtrate into the interstitial
fluid, water cannot follow. Thus, the separation of water reabsorption from salt
reabsorption is achieved. This is required for the regulated reabsorption of water from
the collecting duct by ADH. Inhibiting the active transport of Na+ here would prevent all
of the above.
B. No. Less water can be reabsorbed because there would be a much weaker osmotic
gradient for the water to follow. The filtrate would remain dilute, and a large volume of
dilute urine would be produced.
C. No. Nutrient reabsorption is dependent on active Na + transport in the proximal
convoluted tubule, not the loop of Henle.
D. Wrong. There is active transport of Na+, as explained above.
E. No. This is what happens normally. It requires the active transport of Na + out of the
thick ascending limb.

43. Which of the following hormones are essential for fertility in males?
A. TSH and LH only.
B. TSH and testosterone only.
C. LH and testosterone only.
D. FSH, oestradiol and testosterone.
E. FSH, LH and testosterone.

Answer = E ((L20 and tutorial 5, reproduction). FSH (follicle-stimulating hormone)

stimulates spermatogenesis. LH (luteinising hormone) stimulates testosterone production
from Leydig cells. Testosterone is required for maturation of sperm.
A. Both are required but testosterone is also needed.
B. Both are required but LH is also needed.
C. Both are required but FSH is also needed.
D. FSH and testosterone yes, but oestradiol has no major role in male fertility.
44. What is the function of the corpus luteum?
A. To secrete large quantities of LH and thus prepare the uterus for
implantation of a fertilised egg.
B. To make new egg cells for future cycles.
C. To secrete large quantities of oestradiol and progesterone and thus
prepare the uterus for implantation of a fertilised egg.
D. To secrete FSH and LH in response to GnRH from the hypothalamus.
E. To secrete human chorionic gonadotrophin thus preventing
miscarriage.

Answer = C (L20 and tutorial 5, reproduction). The corpus luteum is formed from the
remains of the ovarian follicle after ovulation has occurred. It secretes large quantities of
oestradiol and progesterone during the early stages of pregnancy to ensure successful
implantation and development of the placenta.
A. No. The corpus luteum does not secrete LH. LH comes from the anterior pituitary.
B. No. All female gametes are produced during early fetal development. No new egg cells
are made during adulthood.
D. No. FSH and LH are secreted from the anterior pituitary in response to GnRH from the
hypothalamus.
E. No. hCG is secreted by the implanted blastocyst.

45. From where is cortisol secreted?

A. The anterior pituitary gland.
B. The adrenal medulla.
C. The posterior pituitary.
D. The zona glomerulosa of the adrenal cortex.
E. The zona fasciculata of the adrenal cortex.

Answer = E (L21, adrenal function). Simple fact.

A. No. This is from where ACTH (which stimulates cortisol secretion) comes from.
B. No. this secretes adrenaline.
C. No. This secretes ADH and oxytocin.
D. No. This secretes aldosterone (another steroid hormone).
46. How does cortisol influence fuel homeostasis?
A. It increases glycogenesis in the liver.
B. It increases glucose uptake by adipose.
C. It increases protein synthesis in muscle.
D. It increases gluconeogenesis in the liver.
E. It stimulates secretion of insulin.

Answer = D (L21, adrenal function, tutorial 5). Cortisol is a catabolic hormone. It

stimulates gluconeogenesis as well as breakdown of protein in muscle and lipolysis in
adipose.
A. No. Glycogenesis is an anabolic process.
B. No. This would be an anabolic effect.
C. No it does the opposite.
E. No and insulin is an anabolic hormone. Cortisol opposes the actions of insulin.

47. What are common causes of Cushing’s syndrome?

A. Deficiency of cortisol
B. Tumours secreting too much of either TRH or TSH.
C. Tumours secreting too much of either CRH or ACTH.
D. Insulin resistance.
E. Immunosuppression.

Answer = C (L21, adrenal function). Cushing’s syndrome is characterised by too much

cortisol, usually caused by hypothalamic or pituitary tumours secreting excess CRH or
ACTH.
A. No. Other way around. Too much cortisol.
B. No. TRH and TSH are the hormones that stimulate thyroid hormone production, not
cortisol.
D. No. Insulin resistance is a consequence of excess cortisol, not a cause of it.
E. No. This is also a consequence of excess cortisol, not a cause of it.
48. Which combination can support the greatest breath-holding time?
A. Prior hyperventilation with 100% O2 supplementation.
B. Prior hyperventilation with 5% CO2 supplementation.
C. Prior hyperventilation alone.
D. Supplementing with 100% O2.
E. Taking a maximum breath in before starting the breath-hold.

Answer = A (L23, comparative physiology). Both prior hyperventilation (practical 2) and

breathing 100% will increase breath-holding time, so in combination they produce the
biggest effect. Hyperventilation lowers PCO2 so it takes longer for CO2 to accumulate.
Breathing 100% O2 raises plasma PO2.
B. Prior breathing of air with 5% CO2 already in it would greatly reduce breath-holding
time and may even be dangerous.
C. This will increase breath-holding time but not as much as in combination with 100% O2.
D. This will increase breath-holding time but not as much as in combination with
hyperventilation.
E. This will increase breath-holding time compared to a normal breath in but not as much
as prior hyperventilation.

49. Which of the below is not an adaptation for long diving times in
whales?
A. Several-fold increase in myoglobin content of muscle.
B. Large spleen.
C. Faster heart rate during diving response.
D. Higher lung capacity per Kg body weight.
E. Resistance to low PO2 (hypoxia).

Answer = C (L23, comparative physiology). The diving response in all mammals involves
a slowing of heart rate. In whales, this response is greatly exaggerated.
A, B, D and E are all correct adaptations.
50. If a horse had a cardiac output at rest approximately eight times that
of a human at rest but a very similar mean arterial pressure, what else
must be true?
A. The horse has a heart rate approximately eight times higher than a
human.
B. The horse has a much weaker baroreceptor response than a human.
C. The horse has an approximately eight times lower total peripheral
resistance at rest than a human.
D. The horse has an approximately eight times higher total peripheral
resistance than a human.
E. The horse has a much stronger baroreceptor response than a human.

Answer = C. (L23, comparative physiology). Darcy’s Law: MAP = CO x TPR. If CO is 8

times greater in the horse but MAP is similar, then TPR must be several times lower.
A. No. The trend as body mass increases is for heart rate to be slower. For there to be a
greater CO, stroke volume is several times greater (larger heart).
B. No. Meaningless statement. The horse has the correct baroreceptor response for a
horse!
D. No. If CO was eight times higher and TPR was also eight times higher, then MAP would
be 64 times higher. MAP = CO x TPR.
E. No. Meaningless statement. The horse has the correct baroreceptor response for a
horse!